Alopecia
Basics
Description
- Alopecia: absence of hair from areas where it normally grows
- Anagen phase: growing hairs, 90% scalp hair follicles at any time, lasts 2 to 6 years
- Catagen phase: regression of follicle, <1% follicles, lasts 3 weeks
- Telogen phase: Resting phase lasts 2 to 3 months, 50 to 150 telogen hairs shed per day.
- Classified as scarring (cicatricial), nonscarring (noncicatricial), or structural
- Scarring (cicatricial) alopecia
- Inflammatory disorders leading to permanent hair loss and follicle destruction
- Includes lichen planopilaris, frontal fibrosing alopecia, and discoid lupus erythematosus
- Nonscarring (noncicatricial) alopecia
- Lack of inflammation, no destruction of follicle
- Includes androgenic alopecia, alopecia areata (AA), telogen effluvium, anagen effluvium
- Structural hair disorders
- Brittle or fragile hair from abnormal hair formation or external insult
Epidemiology
Prevalence
- Androgenic alopecia:
- In males, 30% Caucasian by 30 years of age, 50% by 50 years of age, and 80% by 70 years of age
- In females, 70% of women >65 years of age
- AA: 1/1,000 with lifetime risk of 1–2%, men and women affected equally
- Scarring alopecia: rare, 3–7% of all hair disorder patients
Etiology and Pathophysiology
- Scarring (cicatricial) alopecia
- Inflammatory disorders leading to permanent destruction of the follicle
- Slick smooth scalp without follicles evident
- Three major subtypes based on type of inflammation: lymphocytic, neutrophilic, and mixed
- Primary scarring includes discoid lupus, lichen planopilaris, dissecting cellulitis of scalp, primary fibrosing, among others.
- Secondary scarring from infection, neoplasm, radiation, surgery, and other physical trauma, including tinea capitis
- Central centrifugal cicatricial alopecia most common form of scarring hair loss in African American women; etiology unknown but likely secondary to hair care practices
- Nonscarring (noncicatricial) alopecia
- Focal alopecia
- AA
- Patchy hair loss, usually autoimmune in etiology, T cell–mediated inflammation resulting in premature transition to catagen then telogen phases
- May occur with hair loss in other areas of the body (alopecia totalis [entire scalp]), alopecia universalis (rapid loss of all body hair)
- Nail disease frequently seen
- High psychiatric comorbidity (1)
- Alopecia syphilitica: “moth-eaten” appearance, secondary syphilis
- Postoperative, pressure-induced alopecia: from long periods of pressure on one area of scalp
- Temporal triangular alopecia: congenital patch of hair loss in temporal area, unilateral or bilateral
- Traction alopecia: patchy, due to physical stressor of braids, ponytails, hair weaves
- Pattern hair loss
- Androgenic alopecia: hair transitions from terminal to vellus hairs
- Male pattern hair loss: androgen-mediated hair loss in specific distribution; bitemporal, vertex occurs where androgen sensitive hairs are located on scalp. This is a predominantly hereditary condition (2).
- Increased androgen receptors, increased 5-α reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT). This leads to decreased follicle size and vellus hair (2).
- Norwood Hamilton classification type I to VII
- Female pattern hair loss: thinning on frontal and vertex areas (Ludwig classification, grade I to III). Females with low levels of aromatase have more testosterone available for conversion to DHT (3). This carries an unclear inheritance pattern (2).
- Polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia all lead to androgen changes and can result in alopecia.
- Medications (hormone replacement therapy, oral contraceptive pills)
- Drugs (testosterone, progesterone, danazol, adrenocorticosteroids, anabolic steroids)
- Trichotillomania: intentional pulling of hair from scalp; may present in variety of patterns
- Diffuse alopecia
- Telogen effluvium: sudden shift of many follicles from anagen to telogen phase resulting in decreased hair density but not bald areas
- May follow major stressors, including childbirth, injury, illness; occurs 2 to 3 months after event
- Can be chronic with ongoing illness, including SLE, renal failure, IBS, HIV, thyroid disease, pituitary dysfunction
- Adding or changing medications (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, β-blockers, ACE inhibitors, colchicine, cholesterol-lowering medications, etc.)
- Malnutrition from malabsorption, eating disorders; poor diet can contribute.
- Anagen effluvium
- Interruption of the anagen phase without transition to telogen phase; days to weeks after inciting event
- Chemotherapy is most common trigger.
- Radiation, poisoning, and medications can also trigger.
- Telogen effluvium: sudden shift of many follicles from anagen to telogen phase resulting in decreased hair density but not bald areas
- Structural hair disorders
- Multiple inherited hair disorders including Menkes disease, monilethrix, and so forth. These result in the formation of abnormal hairs that are weakened.
- May also result from chemical or heat damaging from hair processing treatments
Genetics
Family history of early patterned hair loss is common in androgenic alopecia, also in AA.
Risk Factors
- Genetic predisposition
- Chronic illness including autoimmune disease, infections, cancer
- Physiologic stress including pregnancy and childbirth
- Poor nutrition
- Medication, chemotherapy, radiation
- Hair chemical treatments, braids, weaves/extensions
General Prevention
Minimize risk factors where possible.
Commonly Associated Conditions
- See “Etiology and Pathophysiology.”
- Vitiligo—4.1% patients with AA, may be the result of similar autoimmune pathways (4)
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Citation
Domino, Frank J., et al., editors. "Alopecia." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2020. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688645/all/Alopecia.
Alopecia. In: Domino FJF, Baldor RAR, Golding JJ, et al, eds. 5-Minute Clinical Consult. Wolters Kluwer; 2020. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688645/all/Alopecia. Accessed June 2, 2023.
Alopecia. (2020). In Domino, F. J., Baldor, R. A., Golding, J., & Stephens, M. B. (Eds.), 5-Minute Clinical Consult (27th ed.). Wolters Kluwer. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688645/all/Alopecia
Alopecia [Internet]. In: Domino FJF, Baldor RAR, Golding JJ, Stephens MBM, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2020. [cited 2023 June 02]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688645/all/Alopecia.
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